Figure 10-7. T2-weighted magnetic resonance imaging of a patient with vascular dementia shows extensive white-matter hyperintensities.

Figure provided by Dr. Bruce L. Miller, UCLA Harbor Medical Center, Los Angeles, CA. Used with permission.

Alzheimer's disease
Is a primary degenerative cerebral disease It is usually insidious in onset and develops slowly ,period can be as short as 2 or 3 years,

The onset can be in middle adult life (Alzheimer's disease of

presenile onset), higher in later life (Alzheimer's disease of senile onset).

There are characteristic changes in the brain:

a marked reduction in the population of neurons appearance of neurofibrillary tangles neuritic (argentophil) plaques, which consist largely of amyloid and granulovacuolar bodies.

Neurochemical : a marked reduction in the enzyme choline

acetyl-transferase, and in other neurotransmitters and neuromodulators.
Dementia in Alzheimer's disease is at present irreversible.

Figure 10-4. Microscopic brain section showing pyramidal cell layer of hippocampus with numerous triangular intraneuronal neurofibrillary tangles [ ] and several senile plaques [ ] (Bielschowsky stain; original magnification x190). Figure provided by Dr. H. V. Vinters, Section of Neuropathology, UCLA Medical Center, Los Angeles, CA, from Vinters et al. 1988. Used with permission.

F01. Vascular dementia

Vascular (formerly arteriosclerotic) dementia which includes multiinfarct dementia, history of TIA with brief impairment of consciousness, fleeting pareses, or visual loss.

Diagnostic guidelines
The presence of a dementia Impairment of cognitive function and focal neurological signs. Insight and judgement may be relatively well preserved.

F01. Vascular dementia

An abrupt onset or a stepwise deterioration, confirmation can be provided only by computerized axial tomography or neuropathological examination. Associated features are: hypertension, carotid bruit, emotional lability with transient depressive mood, weeping or explosive laughter, and transient episodes of clouded consciousness or delirium, often provoked by further infarction. Personality is believed to be relatively well preserved, but personality changes may be evident

Figure 22-1. The prevalence of dementia by age at stroke onset among testable patients (>60 years) with ischemic stroke. Source. Data obtained from Tatemichi et al. 1990.

Differential diagnosis.
Consider: delirium (F05. -); other dementia, particularly in Alzheimer's disease (FOO. -); mood [affective] disorders (F30 F39); mild or moderate mental retardation (F70 - F71); subdural haemorrhage (traumatic (S06.5), nontraumatic (162.0)). F0l .0 Vascular dementia of acute onset Usually develops rapidly after a succession of strokes from cerebrovascular thrombosis, embolism, or haemorrhage. F0l .1 Mufti-infarct dementia This is more gradual in onset than the acute form F0l .2 Subcortical vascular dementia history of hypertension and in CT foci of ischaemic destruction in the deep white matter of the cerebral hemispheres F0l .3 Mixed cortical and subcortical vascular dementia F0l .8 . Other vascular dementia

Diagnostic guidelines
The following features are required for a definite diagnosis: (a)a progressive dementia; (b)a predominance of frontal lobe features with euphoria, emotional blunting, and coarsening of social behaviour, disinhibition, and either apathy or restlessness; (c)behavioural manifestations, which commonly precede frank memory impairment.

F02.8 Dementia in other specified diseases classified elsewhere Includes dementia in: Carbonmonoxide poisoning (T58) cerebral lipidosis (E75. -) epilepsy (G40. -) general paralysis of the insane (A52. 1) hepatolenticular degeneration (Wilson's disease) (E83 .0) hypercalcaemia (E83 .5) hypothyroidism, acquired (E00. -, E02) intoxications (T36 - T65) multiple sclerosis (G35) neurosyphilis (A52. 1) niacindeficiency pellagra] 52) polyarteritis nodosa (M30.0) systemic lupus erythematosus (M32. -) trypanosomiasis (African B56. -, American B57. -) vitamin B12 deficiency ,E53.8) F03.Unspecified dementia

CLINICAL FEATURES Memory Impairment Orientation Language Impairment Personality Changes Psychosis. Other Impairments Psychiatric. Neurological. Catastrophic reaction. Sundowner syndrome.

DIFFERENTIAL DIAGNOSIS
depressive disorder (F30 - F39), delirium (F05); mild or moderate mental retardation (F70 F71); iatrogenic mental disorders due to medication (F06. -). Dementia of the Alzheimer's Type versus Vascular Dementia Vascular Dementia versus Transient Ischemic Attack Delirium Depression Factitious Disorder Schizophrenia Normal Aging

COURSE AND PROGNOSIS

The classic course of dementia is an onset in the patient 50s or 60s, with gradual deterioration over 5 to 10 yearsleading eventually to death. The age of onset and rapidity of deterioration vary among different types of dementia

Psychosocial Factors

TREATMENT
Some cases of dementia are regarded as treatable
The general treatment approach provide supportive medical care, emotional support for the patients and their families, the maintenance of the patient's physical health, . symptomatic treatment Particular attention must be provided to caretakers and family members

When the diagnosis of vascular dementia is made, risk factors

Pharmacological Treatments Currently available treatments psychoactive drugs Tetrahydroaminoacridine (Tacrine) Psychodynamic Factors

AMNESTIC DISORDERS
single symptom of a memory disorder that causes sigcant impairment in social or occupational functioning. EPIDEMIOLOGY Amnesia is most commonly found in alcohol use disorders and head injury. ETIOLOGY Thiamine deficiency. Hypo-glycemia, hypoxia (including carbon monoxide poisoning), and herpes simplex encephalitis ,tumors, cerebrovascular diseases, surgical procedures, or multiple sclerosis plaques General insults to the brain-for example, seizures, electroconvulsive therapy (ECT), and head trauma-. Many drugs benzodiazepines triazolam (Halcion),

CLINICAL FEATURES AND SUBTYPES

(anterograde amnesia - retrograde amnesia). Short term memory and recent memory are usually impaired. Memory for overlearned information the such as childhood experiences, Cerebrovascular Diseases. Multiple Sclerosis Korsakoff's Syndrome

Alcoholic Blackouts
Electroconvulsive Therapy Head Injury Transient Global Amnesia

DIFFERENTIAL DIAGNOSIS. Dementia and Delirium Normal Aging Dissociative Disorders

Factitious Disorders

COURSE AND PROGNOSIS

The specific cause of the amnestic disorder determines the course and the prognosis for a patient.. Transient amnestic disorder with full recovery is common in temporal lobe epilepsy,ECT, the intake of such drugs as benzodiazepines and barbiturate , and resuscitation from cardiac arrest. Permanent amnestic syndromes may follow a head trauma,carbon monoxide poisoning. a cerebral infarction, subarrachnoid hemorrhage, and herpes simplex encephalitis.

TREATMENT

The primary approach is to treat the underlying cause of the amnestic disorder. Psychodynamic Factors The clinician must respect and empathize with patients' need to deny the reality of what has happened. Clinicians must also be wary of being seduced into thinking that all the patient's symptoms are directly related to the brain insult. An evaluation ofpreexisting personality disorders-such as borderline, antisocial, and narcissistic personality disorders-must be part of the overall assessmentThose personality features may become a crucial part of the psychodynamic psychotherapy.

F06.Other mental disorders due to brain damage and dysfunction and to physical disease
The decision to classify a clinical syndrome here is supported by the following: (a)evidence of cerebral disease, damage or dysfunction, or of systemic physical disease, (b)a temporal relationship (weeks or a few months) between the development of the underlying disease and the onset of the mental syndrome;

(c)recovery from the mental disorder following removal or improvement o the underlying presumed cause; (d)absence of evidence to suggest an alternative cause of the mental syndrome (such as a strong family history or precipitating stress).

F06.Other mental disorders due to brain damage and dysfunction and to physical disease

F06.0 Organic hallucinosis F06.1 Organic catatonic disorder F06.2 Organic delusional (schizophrenia-like) disorder F06.3 Organic mood (affective) disorders F06.4 Organic anxiety disorder F06.5 Organic dissociative disorder F06.6 Organic emotionally labile (asthenici) disorder F06.7 Mild cognitive disorder F06.8.Other specified mental disorders due to brain damage and dysfunction and to physical disease F06.9. Unspecified mental disorder due to bmln damage and dysfunction and to physical disease F07.2 Postconcussional syndrome F07.8. Other organic personality and behavioural disorders due t brain disease, damage and dysfunction

EPILEPSY
GENERAL SEIZURE. ABSENCES (PETIT MAL). Partial seizures. Symptoms Preictal symptoms. Ictal symptoms. Interictal Symptoms PERSONALITY DISTURBANCES. PSYCHOTIC SYMPTOMS. VIOLENCE. MOOD DISORDER SYMPTOMS.

IMMUNE DISORDERS AIDS. Systemic Lupus Erythematosus

ENDOCRINE DISORDERS
Thyriod Disorders Parathyroid Disorders Adrenal Disorders (Addison's disease). (Cushing's syndrome) Pituitary Disorders Sheehan's syndrome.